The University of Texas Medical Branch The School of Allied Health Sciences The Physical Therapy Department PHYT 6202 - Basic Spinal Tissue Pathophysiology NTK = Nice to know; not commonly dealt with by PTs ETK = essential to know; pathology commonly dealt with by PT. I. The intervertebral segment A. Constituents 1. Anterior Elements a. Vertebral Bodies b. Intervertebral disk c. Ligaments (1). Anterior longitudinal ligament (2). Posterior longitudinal ligament (3). Interspinous Ligamant (4). Supraspinous Ligament (5). Intertransverse Ligament e. Anterior muscles (Many authors do not include the muscles within the Intervertebral segment) (1). Intersegmental - “deep”, local, (longus colle; Transversus abdominus) (2). Extrasegmental – “global” (Rectus abdominus, sternomastoid) f. Arteries, veins and nerves to these structures. 2. Posterior Elements a. Bony neural arch (1). Laminae (2). Transverse and spinous processes b. Facets and facet joints and tissues c. Spinal cord and meninges (especially the dura) d. Spinal nerve roots e. Intersegmental muscles – “deep”, local, (multifiidi, rotatores) f. Extra-segmental muscles (iliocostalis, semispinalis, etc) g. Ligaments (1). Ligamentum flavum (2). Interspinous ligament (3). Supraspinous ligament g. Arteries, veins and nerves to these structures 3. Lateral elements a. Ribs b. Joints of von Luschka c. Intertranverse ligaments PHYT 6202 - Basic Spinal Tissue Pathophysiology 2 d. Side flexing muscles – (scalene, quadratus lumborum) II. Overview of tissue pathology- A. Pathological mechanisms of injury: Trauma, Posture (chronic sprain, strain and fatigue), Degeneration, Systemic, Combinations B. Trauma 1. Injures mostly the collagenous tissues in spine structures. The inflammation and repair processes of collagen in tissue are usually what guides treatment and management. The time lines of recovery and chances of restoration are different for different types of collagenous tissues depending on their constituency and function. 2. Traumatic mechanisms a. Directions of force – (1). Hyperflexion (anterior hypercompression c posterior distraction), (2). Hyperextension – posterior hypercompression c anterior distraction (3). Hyper side flexion to the R – R hypercompression c L distraction and v.v. (4). Hyper rotation to the L – hypercompression of R facet with distraction of R anterior disk and v. v. (5). Combinations (hyperflexion c rotation hyperextension c rotation); (6). Extrincic mechanisms – (1). Surgery (2). Contusion (3). Deep tissue wounding (gunshot wound, penetrating objects). 3. A good mental exercise for students is to imagine what structures might be injured by each mechanism. 4. In traumatic mechanisms several different tissues are injured simultaneously. Return to function is limitated is the "weakest link", i.e., the tissue that is injured most easily or severely by the trauma; the tissue that heals the slowest or the tissue that less completely. These are often cartilage and nerve. III. Trauma to anterior elements A.. Vertebral body compression fracture http://www.medmedia.com/o11/183.htm (NTK) - most common is anterior wedge fracture; heal readily in healthy host; occur readily in unhealthy host (osteoporosis); Newest treatment is vertebroplasty; serious complication is expansion into spinal canal or local kyphosis causing spinal stenosis. B. Distraction fracture - http://www.medmedia.com/o11/198.htm (NTK) Chance fracture; flexion distraction – PHYT 6202 - Basic Spinal Tissue Pathophysiology 3 C. End plate fracture (see interspongy disk herniation below) (ETK) D. Anterior longitudinal ligament sprain or tear 1. Most often occurs in hyperextension phase of cervical whiplash but can occur with hyperextension (hyperlordosis) of the lumbar spine. 2. Early pathology - rupture of collagen fibers and bonds; bleeding and inflammation; healing collagen cycle. 3. Late pathology - a. Collagen may heal with excessive length (most likely) allowing excessive lordosis or with diminished length producing postural dysfunction. b. Excessive length may allow anterior shearing instability leading to facet joint degeneration. E. Anterior muscle strain and tear (ETK) 1. Mechanisms of injury: Hyperextension, hyperextension with rotation, sometimes contusion. 2. Early pathology= a. Strain = more of a collagenous injury; bleeding and inflammation/repair of collagen. b. Contusion = can have contractile element injury as well as collagen; more bleeding and collagen repair; collagen repairs some of contractile element. in contusion, (c). Spasm, antalgic posture and movement 3. Late pathology = abnormal remodeling; diminished or excessive length. May establish postural dysfunction F. Disk tear (ETK) 1. Sudden intense force on a small area of the intervetebral disk causes a tear; to get a large force on a small area of the healthy disk requires a combination of movement; hyperflexion with rotation; can be hyperextension with rotation. In the hyperextension with rotation mechanism the facet joint can be injured as well as the disk. The facet joint may subsequently become hypomobile straining the disk more with function . a. Lumbar - usually postero-lateral from twisting while bent forward; usually lifting, shoveling, etc. b. Cervical - tear of anterior disk with extension phase of acceleration injury. 2. Immediate pathology a. Release of pain producing substances - Disk is innervated and some pain comes from disk b. When collagen in cartilage is fractured there is a inflammatory response. By products of collagen breakdown can be very irritating to the surrounding structures including nerve roots and dura. PHYT 6202 - Basic Spinal Tissue Pathophysiology 4 c. Annulus is made of collagen and elastin; collagen attempts to heal; probably never reconstitutes itself, especially elastin; may heal with fibrous scar but is very slow. d. Because nucleus pulposis is contained by the annulus under pressure, tear might cause torn annulus to immediately protrude; Annulus might rupture immediately and allow NP to prolapse or extrude. 2. Long term pathology - Disk tear is often not important for what immediately results from the disk injury but what might occur over time after disk tear. Often leads to other problems: a. Weakens annulus so annular bulge or HNP is more likely over time. b. Loss of one control of rotation at the segment. Annulus helps control rotation (with facets, oblique abdominals, and multifidi mm.) so facets might be injured at same time as disk tear or segmental rotational instability might exist after tear subjecting facets to excess wear. c. Disk space may narrow allowing shearing instability. G. "Intraspongy" herniation - (ETK) Nucleus pulposis herniates superiorly or inferiorly through weakness in the inferior or superior cartilage end plate. Most frequent in the lower thoracic area and upper L/S. Causes few acute symptoms. Creates the phenomenon known as "Schmorl's nodes". 1. Results for fall from height into spinal flexion or lifting heavy object in hyperflexed position. 2. Early pathology = healing of bone; fibrosis of invading nucleus. 3. Late pathology=Because disc narrows and segment becomes stiffer segments above and below may develop excessive motion if patients movements require full ROM. H. To injure the structures named above takes significant force when they are healthy. If the same tissues are degenerated, less force can cause significant injury. I. Circulatory and neural elements - The major neural elements are posterior; some anterior ones that can be pathological are: 1. Vertebral artery (NTK) – also considered a lateral element 2. Artery of adamkewicz (NTK) 3. Abdominal aorta (NTK) IV. Trauma to Posterior Elements A. Bone - 1. fracture of neural arch; see Wheeless textbook of orthopedics (NTK) http://www.medmedia.com/o11/145.htm PHYT 6202 - Basic Spinal Tissue Pathophysiology 5 2. Avulsion fracture of the spinous processes - "Clay shoveler's fracture - (NTK) http://www.medmedia.com/o11/143.htm 3. Isthmic Spondylolysis and Spondylolithesis a. Latest theoretical cause is repetitive stress; patient may have inherited tendency. b. Fracture of pars interarticularis with repetitive hyperextension or hyperextension with rotation. c. Spondylolysis – stress fracture unilaterally or bilaterally without separation. d. Spondylolythesis – separation at fracture site with anterior vertebral slipping of L5 on S1. Slipping graded on how much of L5 overlaps S1. B. Ligament sprain (ETK) 1. Distraction - posterior longitudinal, interspinous, supraspinous most often by hyperflexion or combination flexion/rotation. Often in cervical spine with hyper-flexion phase of whiplash. Less often in thoracic and lumbar spine. 2. Immediate pathology= inflammation and repair of collagenous tissue 3. Chronic pathology = ligament may remodel with diminished or excessive length predisposing segment to acceleration of degeneration. 4. Compression or impingment - Interspinous and supraspinous can be pinched by "kissing spinous processes" phenomenon C. Facet joint fractures; dislocation - unilateral or bilateral jumped facet (NTK) http://www.medmedia.com/o11/110.htm D. Facet joint sprain (ETK) 1. Patient history usually separates this disorder from other non- fracture/dislocation causes of facet joint pain. With FJ sprain there is a history of trauma. Pain pattern during movement tests agrees with direction of capsular stretching force. 2. Hyper-flexion sprain (ETK) a. Hyper-flexion stretches the posterior joint capsule; Therefore flexion and/or rotation are most painful; extension is better movement. Often postures in increased lordosis or extension and rotation toward painful side. b. Rotation combined with flexion may sprain facet joint unilaterally. c. Short term pathology - collagenous tissue over strain with usual sequelae; may accompany other hyper-flexion or rotation pathology. d. Long term pathology = facet joint hypo-mobility or hypermobility. PHYT 6202 - Basic Spinal Tissue Pathophysiology 6 e. Hyper-flexion may have a different pathology when the segment has been previously narrowed by degeneration; compression shear of articular cartilage may occur with capsular stretch. 2. Hyperextension sprain (ETK) a. Pt remembers hyperextension episode, with or without rotation. b. Extension with or without rotation is most painful; flexion is better movement. c. Short term pathology; usual sequelae of collagenous capsular damage. Additional pathology of hyperextension may be articular cartilage damage (cartilage damage may "extend the life" of inflammatory response due to collagen degradation cycle; hyperextension may also impinge posterior capsule. d. Long term pathology = muscle fatigue due to antalgic posturing in flexion. 3. Facet joint capsular impingement (ETK) - This pathology can be the result of trauma with excessive force but often occurs with slight (some would say normal) movements. It is included here because it usually occurs with a sudden onset. Impingement occurs when a portion of the joint capsule becomes folded and entrapped inside the joint. It can be part of the synovial lining, and some call it a "meniscoid body". A meniscoid body is part of the synovial structure. Twomey has suggested "meniscoid bodies" are detachment of the multifidus mm from previous injuries. (A slip of the multifidus muscle often blends with the joint capsule much like the rotator cuff muscles at the shoulder). a. Immediate pathology = release of pain producing substance; irritation of joint capsule (one of the most mechano-sensitive tissues when inflamed). Antalgic positioning and movement. Often patient will attempt to self manipulate and pinch the capsule more. Gradual recovery over time with capsule "wiggling" its way out of the capsule. b. Long term pathology = antalgic posturing and movement can establish pain/spasm cycle in guarding muscles. (c). Degeneration narrows the disk space and facet joint capsules can slacken. This may make impingement more likely. E. Nerve injury 1. Central nervous system structures a. In hyper-mobile persons, hyper-flexion can traction the spinal cord without serious damage to the segments. http://www.medmedia.com/o11/176.htm PHYT 6202 - Basic Spinal Tissue Pathophysiology 7 (1). Immediate pathology = spinal cord shock; bleeding and inflammation among fibers of cord (2). Long term pathology = muscle paresis or paralysis; diminished or absent sensation and neurological control b. Large central traumatic protrusion can pressure the spinal cord or cauda equina. (1). Immediate pathology = pressure disturbance in conduction through cord (cervical and thoracic) can be as minor as tingling in hands and feet or as major as paralysis: cauda equina in lumbar area (tingling to loss of sensation and motor power; loss of bowel and bladder) (2). Long term pathology= as above 2. Peripheral nerve injury a. Traction or Compression of nerve plexus (usually the brachial plexus) -.(NTK) AKA burner syndrome http://www.medmedia.com/t1/150.htm (1). Mechanisms – Head/neck side flexion with ipsilateral shoulder depression; hyper side flexion to same side; shoulder hyper abduction with traction. (2). Immediate pathology = injury to collagenous elements; swelling; actual destruction or dissassociation of nerve fibers; slowing or altering conduction. (3). Long term pathology - Study showed that 70% of college football players had residual symptoms. b. Nerve root injury (1). Injury mechanism = Closing of spinal canal by disk (thoracic and lumbar); Closing of intervertebral foramen by disk, facet, descending pedicle (all areas) (2). Immediate pathology (a). Injury to collagenous elements produce swelling. Swelling affects myelin slowing or elimination of conduction from myelinated fibers. Direct mechanical stimulation creates messages as if fiber were conducting from the receptor. Can create imbalance at “gate” favoring C fiber input. (b). Nerve root ischemia – traumatic incident may injure blood supply slowing or limiting its ability to heal. The nerve is contained within a somewhat unyielding fibrous sheath. As nerve swells, it may compromise its own blood PHYT 6202 - Basic Spinal Tissue Pathophysiology 8 supply. Ischemic nerve root are acutely mechano sensitive. (See Kessler, p. 552-3 plus ligature article by Smyth and Wright) (3). Long term pathology (a). Collagenous scar may form within the nerve or around the nerve (adhesion to less yielding tissues in the area); may lead to decreased nerve excursion (attempts to elongate nerve to its normal length renders nerve ischemic). (b). Collagenous tissue element (as opposed to the conductive tissue) may remodel short. (attempts to elongate nerve to its normal length renders nerve ischemic).. F. Posterior Muscle Injury (ETK) 1. Mechanism = Strain: eccentric hyper-flexion or flexion c rotation; strong isometric while in flexion or flexion c rotation; lifting injuries. Hyper-flexion phase of whiplash; Contusion: direct blow to muscles; Surgical incisions 2. Short term pathology = Strains are usually more of a collagenous injury and follow that path; Contusions can be more injury to contractile part and there would be more bleeding and repair of contractile portion with fibrous scar. 3. Long term pathology a. Pain/spasm cycle - b. Fibrous scar and adhesions c. Muscle weakness and endurance – decreased ability to perform functional movements; painful fatigue with “normal range loading”. d. Muscle imbalance – joints work with faulty PICR e. Deficient joint stabilization V. Postural Pathology A. Mechanisms - inherited, congenital, habitual, acquired, vocational, avocational repetitive postures and movements cause muscles and other supporting tissues to remodel with excessive length, diminished length, less than normal strength, greater than normal strength. 1. Well-recognized total body patterns in the sagittal plane (Think of these as forms of column buckling under the constant downward pressure of gravity) a. Hyperlordotic/Hyperkyphotic b. Sway back c. Flat back 2. Well-recognized sagittal head/neck/shoulder postures PHYT 6202 - Basic Spinal Tissue Pathophysiology 9 a. Forward head c excessive lordosis; often part of Hyper- lordotic/Hyper-kyphotic pattern. b. Forward head c straight neck and posterior cranial rotation; shoulder protraction; often part of sway back. 3. Well-recognized frontal/horizontal patterns a. Unilateral short leg (actual and functional) b. Scoliosis - http://www.medmedia.com/o11/59.htm c. Torticollis - side flexion- rotation opposite in cervical spine - http://www.medmedia.com/o11/124.htm B. Early Pathology 1. Accumulation of fatigue waste products in tissues; especially constantly contracting muscles; creep in collagenous tissues that are maintained in elongated state (breaking of bonds; denaturing of collagen); stress deprivation in tissues constantly on slack. 2. Stress deformation of articular cartilage surfaces held in constant contact C. Late Pathology 1. Collagen remodeling either with excessive length or diminished length depending on demand. 2. Shift in length-tension curve in contractile element a. Lower peak force/earlier if muscle used in shorter range b. Higher peak force/later if muscle used in excessive length range. 3. Postural dysfunctions may be related to degenerative conditions a. Hyperlordotic/Hyperkyphotic - (1). may increase forward shearing forces in lordotic areas (cervical and lumbar area to encourage the development of degenerative spondlyolithesis http://www.medmedia.com/o11/106.htm (2). Facet joint fatigue or chronic sprain (a). Special designation used to describe pain that seems to emanate from the facet joints but the mechanism is not traumatic. (b). Assumed to be related to chronic overuse in repetitive twisting of the spine and chronic postural hyper-compression sprain. Often worse in pts with advanced segmental degeneration. b. Flat back - (1). Chronic loading of lumbar spine in flexion may lead to gradual degeneration of posterior annulus due to constant backward pressure of the nucleus c. Sway back (1). Chronic facet joint compression fatigue at lumbo- sacral junction; flexion degeneration of disk above lowest level PHYT 6202 - Basic Spinal Tissue Pathophysiology 10 d. Forward head c straight neck (1). Compression fatigue in upper cervical areas. (2). Disk degeneration at lower levels e. Forward head c lordosis (1). Facet joint compression fatigue in middle segments (2). Encourages forward shear at segments VI. Degenerative Pathology A. Basic Assumption regarding the Spinal Segments. The natural history of the intervertebral segment is that all humans develop degenerative segments that first become unstable and then eventually become re-stabilized. Some persons may be genetically predisposed to accelerated degeneration and development of symptoms. (Tissue turnover, shape of spinal canal, asymmetrical facets, pain suppression deficiency, postural dysfunction, etc.) Some may acquire conditions through life that accelerated degeneration and create symptoms (disk tear, facet joint hypomobility, hypermobility, and hypertrophy; de-conditioning, postural dysfunction. Most undergo this process with tolerable symptoms. http://www.medmedia.com/lib6/107.htm 2. Almost any pathology that can result from trauma, can result from similar mechanisms repeated with lighter forces given enough time and cycles of application. VII. Degenerative pathology of the anterior elements A. Osteophytes of the vertebral body 1. Mechanism - instability and disk space narrowing cause ligaments and annulus to slacken; instead of tightening gradually, they tighten suddenly subjecting attachments to stress. Bone will hypertrophy at site of attachment as a stress reaction. 2. Long-term pathology a. Anterior osteophytes - Often causes no painful pathology when osteophytes are anterior because they do not press on pain producing structures. Are often misleading in radiographs (false positive for serious pathology) Occasionally persons with anterior osteophytes in the neck have voice changes and have difficulty swallowing. Anterior osteophytes in the lumbar spine can irritate the descending aorta. Anterior body osteophytes have been known to friction the sympathetic chain in the thoracic spine. b. Posterior osteophytes – Have the greatest potential for causing pathology. Can pressure neural structures in the central canal or in the intervertebral foramen. Are often a contributor to central or lateral spinal stenosis. PHYT 6202 - Basic Spinal Tissue Pathophysiology 11 c. Lateral osteophytes - osteophytes developing off the joints of von Lushka in the cervical spine can have pressure on the vertebral artery which can cause drop attacks. B. Anterior longitudinal ligament remodeled with excessive length 1. Mechanism = chronic Hypl-Hypk postural dysfunction; hyperextension injury. 2. Short term pathology = allows forward shear of top vertabra relative to bottom; facet joint irritation; loss of one of many controls over rotation. 3. Long term pathology a. With forward shear at segment and chronic hyper- compression, facet joints become pathological with synovial hypertrophy; hypermobility; cartilage wear; and hypertrophy; facet joint hypertrophy can (along with other pathology) narrow IVF and pinch nerves. C. Degenerative inter-vertebral disk pathology 1. Mechanism = http://www.medmedia.com/lib3/213.htm a. Natural history of disk, i.e., nucleus becomes more fibrous; collagen turn over slows so slight damage is not repaired. b. Habits, occupation, body mechanics that distribute pressure of nucleus unevenly on annulus. (1). Chronic HypL-HypK standing posture - Anterior protrusion (2). Sitting, repeated bending, flat back posture - Posterior protrusion (3). Occupations or sports with repeated rotation. c. Assymetry of segmental movement (1). Unilateral facet hypomobility (2). Unilateral facet hypermobility (3). Assymetrical facets (4). Adjacent to hypomobile segments d. Loss of control over rotation (1). Abdominal oblique weakness (2). Multifidus weakness (3). Excessive ligament length 2. Internal disk disruption – AKA “black disk disease” because of its appearance on certain MRI studies due to loss of water content. a. Accelerated aging of the disk b. End plate disruption – diminished nutrition of the disk c. Cracks and fissures in the annulus d. Nucleus Pulposus becomes more fibrotic; loses GAGs and does not bind water. PHYT 6202 - Basic Spinal Tissue Pathophysiology 12 e. Usually allows disk space to narrow; annulus slackens; ligaments slacken (at least temporarily); segment becomes unstable with A-P shear and rotary shear. Pathology is usually from the other segmental structures that undergo strain due to loss of stability (facets, facet joint capsules, ligaments, etc). f. Nucleus may or may not herniated the annulus 3. Disk disruption with herniation (Posterior lateral is shown but herniation can occur in other part of the disk) a. Normal Disk (1). Annulus contains nucleus pulposus under pressure (a). NP is constantly trying to expand (b). A condition that exists in the first 4-5 decades (c). Disk is a ligament that helps control rotation and shear. b. Early Pathology (1). Stage 1 - Develops gradually as radial and circumferential tears develop in the disk due to faulty mechanics and overstress. (a). Disk may become mildly symptomatic - intermittent back pain; often assymptomatic. (b). Disk is less able to control rotation and shear; other segmental structures may become symptomatic. (2). Stage 2 - Nucleus pulposus is contained by the annulus under great pressure; gradually works its way peripherally through the annulus. (a). Annulus bulges when disk is compressed under pressure and may produce symptoms. When not compressed may be symptomatic (b). Disk is disrupted and may allow abnormal shear or rotation; symptoms from other segmental structures. http://www.medmedia.com/a5/115.htm PHYT 6202 - Basic Spinal Tissue Pathophysiology 13 (3). Stage 3 (annular bulge) - NP actually causes a peripheral bulge. At this point disk pathology usually becomes symptomatic. Proteolytic enzymes from cartilage damage and pain producing substances from collagen damage irritate pain sensitive tissues that are toward the periphery of the disk. Ligament tissue may be irritated, dura and nerve sleeve. (4). When disk bulge reaches stage 3 they can take three basic sizes (a). Small (intermittent) (b). Medium (intermittent and constant) (c). Large (usually constant) (5). Annular bulge can occur in three locations of a disk (a). Anterior disk protrusion (ADP) - The NP may work its way anteriorly in which case it may be somewhat benign in terms of directly producing symptoms but not benign in terms of producing secondary symptoms related to segmental instability. (b). Near Lateral Postero-lateral disk protrusion - The NP may work toward postero- lateral disk just lateral to the posterior lateral ligament. This location is said to comprise 80% of the immediate symptom producing DP's. (c). Far Lateral Postero-lateral disk protrusion - Protrusion occurs more lateral than Near Lateral and produces slightly different symptoms and different prognosis. (6). Near Postero-lateral protrusions can sequentially pressure and friction the following structures with resulting inflammatory signs and symptoms: Posterior Longitudinal Ligament, Dura, Dural sleeve, nerve root. PHYT 6202 - Basic Spinal Tissue Pathophysiology 14 (7). Stage 4 - Annulus ruptures. NP extrudes or becomes sequestrated. (More common in L/S less common in C/S due to wider ligament; less room to accommodate large protrusion; pt's seek treatment earlier). (a). Early pathology for stage 4 - Nucleus material is interpreted as a "foreign body" and causes a strong inflammatory reaction by the immune cells in the area. Since that area is around the nerve root it often causes intense discomfort from the nerve root. Because the NP is a softer object frictioning the nerve root there is some relief from the pathology associated with pressure and frictioning of the nerve root. (b). Long term pathology - since it is interpreted as a foreign object, the NP is completely digested and dissolved. Unfortunately a fibrous scar can be left to adhere the nerve root to surrounding unyielding tissues. 4. Not all disk postero-lateral protrusions cause symptoms. There is not a direct correlation between severity of a patient's disk degeneration and signs and symptoms produced. http://www.medmedia.com/lib6/107.htm a. Reasons assymptomatic or symptomatic PL HNP may be: (1). Size of spinal canal (2). Size of intervertebral foramen (3). Shape and size of pedicles (4). Pre-existing instability (5). Pre-existing degeneration (6). Pain suppression abilities (7). Postural dysfunction 5. Late Pathology of disk protrusion a. The disk is as much a ligament helping control rotation at the segment as much as a separator between vertebra. Loss of control over rotation will subject the facet joints to increased pressure and probable degeneration. The same is true for strain on ligaments controlling rotation. If over rotation occurs the nerve roots can be damaged. PHYT 6202 - Basic Spinal Tissue Pathophysiology 15 b. As nucleus moves toward the periphery or is lost through a tear in the annulus, the disk space narrows; pedicles descend, IVF narrows, ligaments and annulus slacken. c. Continued pressure on nerve root by a bulging annulus can change its conductivity permanently. d. Cartilage degeneration produces vigorous inflammation that eventually heals with scar tissue. The scar tissue can cause adhesions between nerve roots and surrounding structures. 6. Discitis – infection of the disk a. Systemic – organism introduced to disk by circulation b. Iatrogenic – post discogram; partial disectomy c. Inflammation and repair of the disk (1). Disk could expand posteriorly into spinal canal to cause neural signs and symptoms. (2). Segment usually left with narrowing and instability. D. Anterior muscle weakening, decreased endurance, length changes. 1. Degenerative process causes discomfort; discomfort often reduces activity level 2. Imbalance develops between key muscles that exert mutual control. These are the abdominals with hip flexors and deep neck flexors with sterno-mastoid (former gets weak and elongated, later gets tight and strong). This imbalance encourages A-P shearing at segments. 3. Muscle helping ligaments, disk and facets control rotation weaken with avoidance of movement. Loss of this control over rotation puts greater load on other rotation control structures and they in turn fail. VIII. Degenerative pathology of the posterior elements. A. Pedicles 1. Upper pedicle descends toward the lower as disk space narrows. Since nerve roots are directly under the pedicle, it becomes a source of pressure. 2. Pedicles hypertrophy; perhaps because of excessive pressure B. Degenerative Spondylolythesis – AKA osteoarthritis, spondylosis, DJD of the segment; Intermittent Lateral stenosis; Central stenosis. 1. Disk disruption; slackening of ligaments; change in shape of facets. Usually L4 slips forward on L5 (posterior neural arch intact). 2. Narrows both central canal and intervertebral foramen not usually a part of the segmental degeneration process of DJD development. PHYT 6202 - Basic Spinal Tissue Pathophysiology 16 3. Can be subtle and easily manageable by PT or severe requiring surgical decompression and/or stabilization. C. Facet joint capsular hypertrophy 1. With disk space narrowing, facet joint capsules slacken and "bunch up". 2. With excessive pressure on articular cartilage there is flaking of collagen. Synovial tissue reacts and must be excessively active. (It is synovial tissue's job to keep joint fluid clear of collagen during normal turnover of articular cartilage). Since tissue is hyperactive it hypertrophies. Assumed to be more prone to impingement. 3. Synovial cyst – pinching enlargement of synovial cycle with accumulation of fluid in cyst. Can be large enough to cause nerve pressure. D. Facet joint articular cartilage osteoarthritis 1. With excessive pressure and abrasion of articular cartilage with segmental instability, there is more articular cartilage damage than occurs with normal turnover. 2. Articular cartiage thins, develops fissures and may erode completely. E. Facet joint bony hypetrophy – AKA “re-stabilization” 1. A response to articular cartilage thinning is bony hypertrophy under the cartilage. Bone becomes more dense under the cartilage. 2. Another typical osteoarthritis response due to joint instability is for the joint surface to broaden, to make more surface area. This is seen as an attempt to "re-stabilize" the joint. 3. Broadening of the joint surface is around the edges and are often called osteophytes. Osteophytes of the facet joints are often a source of intervertebral narrowing which can subject the nerve root to trauma. F. Slackening of ligaments 1. With disk space narrowing ligaments slacken. If a collagenous tissue slackens it normally remodels short and "re-tightens" but at a shorter length. 2. Because the segment is slack and often shifts pulling sharply on ligaments, it is assumed that this keeps ligaments from remodeling short and helping re-stabilize the segment. Of course, if posterior ligament does remodel short it would increase lordosis and help to narrow the intervertebral segment. 3. Slack ligaments allows shearing and excessive rotation. 4. Ligamentum flavum - One ligament that is usual is the ligamentum flavum. This ligament folds inward between the lamina PHYT 6202 - Basic Spinal Tissue Pathophysiology 17 and can narrow the spinal canal subjecting either the spinal cord or cauda equina to pressure. One of many elements causing central or lateral stenosis. IX. Segmental Instability 1. Segmental stability is the result of optimal function of three interdependent subsystems a. The passive subsystem – Ligaments, bone, disk, facets b. The active subsystem – muscles (1). Deep intersegmental muscles (2). More superficial global muscles c. The neural subsystem – The motor commands from the CNS that gives muscles their proper amplitude and relative timing. d. Gross deficiency in any one system leads to gross instability. e. Subtle deficiencies in any one sub-system can be compensated by up-regulation of the others (the basis of exercise therapy). f. Subtle deficiencies un-compensated can lead to segmental degeneration. 2. The neutral zone concept (not to be confused with the neutral spine position). a. A small area somewhere between the extremes of motion in each degree of freedom of segmental motion. b. Passive structures and global muscle control the spine (limit excessive or possibly injurious movement outside the neutral zone. In doing they set the limits of the neutral zone. c. Intersegmental muscles control the spine in the neutral zone, i.e., they can stiffen or let loose the segment appropriate for the activity. d. Injury or poor function of these structures allows an expansion of the neutral zone. Intersegmental muscles are required to control a larger movement and sometimes this demand is greater than their capability. e. Dysfunction of intersegmental muscles allows for poor control of movement in the neutral zone. This can be a subtle source of stress and strain on segmental tissues leading to pain and degeneration. f. Global and local (intersegmental) muscles should be coordinated in action with the global muscles moving the spine or controlling large forces applied to the trunk while the local muscles stabilize the segment. 3. Post-surgical Instability a. Some types of discotomy without fusion cause a decrease in disk height creating segmental instability. b. Surgery is performed even with fusion of a segment. If patient keeps same muscle tightness and weakness patterns as pre-surgery two things may happen: PHYT 6202 - Basic Spinal Tissue Pathophysiology 18 (1). Surgery fails after initial success. (2). Segments above or below undergo excessive stress inducing instability. X. De-conditioning A. Relative de-conditioning – a state where muscles and other tissues lack strength/endurance; length required of usual ADL, the persons chosen IADLs plus a reserve for emergencies. B. Morbid de-conditioning – a state where muscles and other tissues lack strength/endurance; length required of usual ADLs so that performing ADLs is dangerous to homestasis. C. Spinal Pathology related to deconditioning 1. Segmental instability and degeneration 2. Postural dysfunction 3. Movement dysfunction 4. Delayed muscle soreness 5. Muscle strain or ligament sprain XI. Dysfunctional movement A. Movement habits or patterns that have been related to risk of injuring spinal tissues. Activities often requiring modification. 1. Supine to sit 2. Floor to waist lift 3. Overhead lift 4. Reaching forward or forward and down 5. Bending forward 6. Sitting working at a desk 7. Sit to stand 8. Sitting posture 9. Standing posture 10. Lying postures 11. Turning while holding an object of weight. 12. Entering and exiting a car. 13. IADLs as required. XII. Systemic pathology – pathologies that can cause spinal pain. PT either modifies plan considering pathology or makes the appropriate referral. A. Cervical, Abdominal, Thoracic, and Pelvic organ disease PHYT 6202 - Basic Spinal Tissue Pathophysiology 19 B. Cardio-vascular disease C. Neurological and disease D. Obesity E. Deconditioning F. Cancer and metasteses G. Depression H. Chronic fatigue I. Chronic Pain Conditions 1. Failure of pain suppression mechanisms a. Peripheral – changes in the posterior horn whereby wide dynamic range fibers conduct pain only. b. Central failure – exhaustion of or failure to produce sufficient endorphins, enkephalins, etc. 2. Myofascial Pain Syndrome 3. Fibromyalgia 4. Failed Back Surgery Syndrome a. Causes 1. Nerve root scarring (inside canal, intervertebral foramen, intermuscular) 2. Arachnoiditis - inflammation of meniges 3. Segmental instability (degeneration above or below fusion) 4. Psycho-emotional response in patient who was not a good candidate 5. Low Back Pain Syndrome a. Psycho-emotional disorder typified by pain and suffering behaviors. b. Physical source cannot be found by usual investigative means. c. Sometimes responds to psycho-therapy, relaxation training, myo-fascial treatment, patient education, job retraining and eventually leading to exercise reconditioning.